Chronic kidney disease (CKD) is a progressive disease that affects > 10% of the total population worldwide or >800 million people. CKD poses a particularly heavy burden in low- and middle-income countries, which are least able to cope with its consequences. It has become one of the leading causes of death worldwide and is one of the few non-communicable diseases where the number of related deaths has increased over the last two decades. The high number of people affected, and the significant negative impact of CKD should be a reason to increase efforts to improve prevention and treatment. The interaction of lung and kidney leads to highly complex and difficult clinical scenarios. CKD significantly affects the physiology of the lung by altering fluid homeostasis, acid-base balance and vascular tone. In the lung, haemodynamic disturbances lead to the development of alterations in ventilatory control, pulmonary congestion, capillary stress failure and pulmonary vascular disease. In the kidney, haemodynamic disturbances lead to sodium and water retention and the deterioration of renal function. In this article, we would like to draw attention to the importance of harmonising the definitions of clinical events in pneumology and renal medicine. We would also like to highlight the need for pulmonary function tests in routine clinical practise for the management of patients with CKD, in order to find new concepts for pathophysiological based disease-specific management strategies.

In many immune-mediated kidney diseases, tissue injury is driven by dysregulated B-cell immunity, with autoantibodies and complement acting as key effectors at the glomerulus. Corticosteroids and conventional immunosuppressants control these diseases only in part, and they do so at the price of cumulative toxicity and frequent relapse. Anti-CD20 antibodies deplete circulating B cells but spare plasmablasts and CD19+ plasma cells that sustain autoantibody production, leaving a residual autoreactive compartment that may contribute to refractory disease and relapse. Anti-CD19 chimeric antigen receptor (CAR) T cells target a broader spectrum of B-cell populations, and early clinical studies suggest that this deeper depletion extends into secondary lymphoid tissues. The clinical evidence, however, is uneven. It is strongest in systemic lupus erythematosus and refractory lupus nephritis, where case series and early-phase trials report clinical and serological remission together with discontinuation of immunosuppression and treatment-free remission. In multiple myeloma and immunoglobulin light-chain (AL) amyloidosis with renal involvement, anti-B-cell maturation antigen (anti-BCMA) CAR-T products are increasingly used in real-world cohorts of patients with reduced estimated glomerular filtration rate (eGFR) or on dialysis, while bispecific T-cell engagers such as teclistamab offer an off-the-shelf alternative. The toxicity of these agents concerns the nephrologist directly. Cytokine release syndrome, immune effector cell-associated neurotoxicity syndrome, tumor lysis syndrome, and the immune effector cell-associated hemophagocytic lymphohistiocytosis-like syndrome (IEC-HS) (IEC-HS) can each involve the kidney, as can the newly defined local immune effector cell-associated toxicity syndrome (LICATS). This review explores the immunological basis of CAR-T constructs, the evidence by disease, the renal toxicity profile, and the criteria for candidate selection and nephrological monitoring.